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Signaling and the Progression of Coronary Vessel Formation
Author(s) -
Tomanek Robert
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.62.2
Subject(s) - vasculogenesis , angiogenesis , microbiology and biotechnology , fibroblast growth factor , biology , medicine , cancer research , receptor , stem cell , progenitor cell
Formation of the coronary vasculature requires the transformation and differentiation of cells that originate in the proepicardium and form the epicardium. The latter provides the cells that comprise the coronary vessels: endothelial, smooth muscle and pericytes. The first primitive (non‐perfused) vasculature consists of endothelial tubes that develop via vasculogenesis. They branch and also fuse with adjacent tubes to form larger channels. The regulation of these events involves many regulating molecules, e.g., GATA, Wilm's Tumor 1, and VEGF and FGF family members. Recent studies document the interdependency of growth factors in this process and indicate that that at least 6 FGFs (1, 2, 4, 8, 9, 18) promote endothelial cell proliferation and tube formation primarily, but not exclusively via FGFR1 signaling. FGF is a key player in the activation of hedgehog which stimulates VEGF signaling. Moreover, stimulation of tubulogenesis requires the availability of both FGF and VEGF. Although VEGF‐A and VEGFR‐2 are important for vasculogenesis and angiogenesis, VEGF‐B and its receptor, VEGFR‐1 as well as VEGF–C each contributes to coronary vessel development. Formation of the coronary ostia and main coronary arteries requires VEGF signaling at the precise sites on the aorta where the capillary plexus penetrates the wall of the artery to establish perfusion of the coronary vasculature. Smooth muscle recruitment to the vascular channels is facilitated by FGFs, VEGFs, TGF‐β. These signaling events are temporally and spatially regulated and are also influenced by other factors, e.g., neural crest cells, and tissue O 2 levels.